ROLE OF NITRIC OXIDE IN THE CARDIAC CONTRACTILE DYSFUNCTION WHICH OCCURS AFTER INTESTINAL ISCHEMIA, and REPERFUSION

Shock ◽  
1995 ◽  
Vol 3 (6) ◽  
pp. 19
Author(s):  
J. T. Murphy ◽  
J. W. Horton ◽  
D. J. White
Keyword(s):  
Nitric Oxide ◽  
Intestinal Ischemia ◽  
Contractile Dysfunction ◽  
Ischemia And Reperfusion ◽  
Cardiac Contractile ◽  
Cardiac Contractile Dysfunction

scholarly journals Endocannabinoids acting at CB1receptors mediate the cardiac contractile dysfunction in vivo in cirrhotic rats

2007 ◽  
Vol 293 (3) ◽  
pp. H1689-H1695 ◽  
Author(s):  
Sándor Bátkai ◽  
Partha Mukhopadhyay ◽  
Judith Harvey-White ◽  
Raouf Kechrid ◽  
Pál Pacher ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Liver Cirrhosis ◽  
Cardiac Contractility ◽  
Receptor Expression ◽  
Contractile Dysfunction ◽  
Cirrhotic Cardiomyopathy ◽  
Cardiac Contractile ◽  
Cardiac Contractile Dysfunction

Advanced liver cirrhosis is associated with hyperdynamic circulation consisting of systemic hypotension, decreased peripheral resistance, and cardiac dysfunction, termed cirrhotic cardiomyopathy. Previous studies have revealed the role of endocannabinoids and vascular CB1receptors in the development of generalized hypotension and mesenteric vasodilation in animal models of liver cirrhosis, and CB1receptors have also been implicated in the decreased β-adrenergic responsiveness of isolated heart tissue from cirrhotic rats. Here we document the cardiac contractile dysfunction in vivo in liver cirrhosis and explore the role of the endocannabinoid system in its development. Rats with CCl4-induced cirrhosis developed decreased cardiac contractility, as documented through the use of the Millar pressure-volume microcatheter system, low blood pressure, and tachycardia. Bolus intravenous injection of the CB1antagonist AM251 (3 mg/kg) acutely increased mean blood pressure, as well as both load-dependent and -independent indexes of systolic function, whereas no such changes were elicited by AM251 in control rats. Furthermore, tissue levels of the endocannabinoid anandamide increased 2.7-fold in the heart of cirrhotic compared with control rats, without any change in 2-arachidonoylglycerol levels, whereas, in the cirrhotic liver, both 2-arachidonoylglycerol (6-fold) and anandamide (3.5-fold) were markedly increased. CB1-receptor expression in the heart was unaffected by cirrhosis, as verified by Western blotting. Activation of cardiac CB1receptors by endogenous anandamide contributes to the reduced cardiac contractility in liver cirrhosis, and CB1-receptor antagonists may be used to improve contractile function in cirrhotic cardiomyopathy and, possibly, in other forms of heart failure.

NITRIC OXIDE SYNTHASE IS NOT INVOLVED IN CARDIAC CONTRACTILE DYSFUNCTION IN A RAT MODEL OF ENDOTOXEMIA WITHOUT SHOCK

Shock ◽  
1997 ◽  
Vol 7 (2) ◽  
pp. 111-118 ◽  
Author(s):  
Xianzhong Meng ◽  
Lihua Ao ◽  
James M. Brown ◽  
Dave A. Fullerton ◽  
Anirban Banerjee ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Rat Model ◽  
Contractile Dysfunction ◽  
Cardiac Contractile ◽  
Cardiac Contractile Dysfunction ◽  
Oxide Synthase

Molecular and pharmacological approaches to inhibiting nitric oxide after burn trauma

2003 ◽  
Vol 285 (4) ◽  
pp. H1616-H1625 ◽  
Author(s):  
Jean White ◽  
Deborah L. Carlson ◽  
Marita Thompson ◽  
David L. Maass ◽  
Billy Sanders ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiac Function ◽  
Total Body Surface Area ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Contractile Dysfunction ◽  
Wild Type ◽  
Burn Trauma ◽  
Cardiac Contractile ◽  
Cardiac Contractile Dysfunction

Whereas controversial, several studies have suggested that nitric oxide (NO) alters cardiac contractility via cGMP, peroxynitrite, or poly(ADP ribose) synthetase (PARS) activation. This study determined whether burn-related upregulation of myocardial inducible NO synthase (iNOS) and NO generation contributes to burn-mediated cardiac contractile dysfunction. Mice homozygous null for the iNOS gene (iNOS knockouts) were obtained from Jackson Laboratory. iNOS knockouts (KO) as well as wild-type mice were given a cutaneous burn over 40% of the total body surface area by the application of brass probes (1 × 2 × 0.3 cm) heated to 100°C to the animals' sides and back for 5 s (iNOS/KO burn and wild-type burn). Additional groups of iNOS KO and wild-type mice served as appropriate sham burn groups (iNOS/KO sham and wild-type sham). Cardiac function was assessed 24 h postburn by perfusing hearts ( n = 7–10 mice/group). Burn trauma in wild-type mice impaired cardiac function as indicated by the lower left ventricular pressure (LVP, 67 ± 2 mmHg) compared with that measured in wild-type shams (94 ± 2 mmHg, P < 0.001), a lower rate of LVP rise (+dP/d tmax, 1,620 ± 94 vs. 2,240 ± 58 mmHg/s, P < 0.001), and a lower rate of LVP fall (–dP/d tmax, 1,200 ± 84 vs. 1,800 ± 42 mmHg/s, P < 0.001). Ventricular function curves confirmed significant contractile dysfunction after burn trauma in wild-type mice. Burn trauma in iNOS KO mice produced fewer cardiac derangements compared with those observed in wild-type burns (LVP: 78 ± 5 mmHg; +dP/d t: 1,889 ± 160 mmHg/s; –dP/d t: 1,480 ± 154 mmHg/s). The use of a pharmacological approach to inhibit iNOS (aminoguanidine, given ip) in additional wild-type shams and burns confirmed the iNOS KO data. Whereas the absence of iNOS attenuated burn-mediated cardiac contractile dysfunction, these experiments did not determine the contribution of cardiac-derived NO versus NO generated by immune cells. However, our data indicate a role for NO in cardiac dysfunction after major trauma.

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